An implantable cardiac rhythm management device is a type of implantable medical device (IMD) that delivers therapy to the heart of a patient in which the device is implanted. For example, a pacemaker recognizes various cardiac arrhythmias and delivers electrical pacing pulses to the heart in an effort to remedy the arrhythmias. An implantable cardioverter/defibrillator (ICD) additionally or alternatively recognizes ventricular tachycardia (VT) and ventricular fibrillation (VF) and delivers electrical shocks or other therapies to terminate these ventricular tachyarrhythmias. At least some pacemakers and ICDs are also equipped to deliver CRT to the heart of the patient. Briefly, CRT seeks to normalize the dyssynchronous cardiac electrical activation and resultant dyssynchronous contractions associated with congestive heart failure (CHF) by delivering synchronized pacing stimulus to both sides of the left ventricle using left ventricular (LV) and right ventricular (RV) leads. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT-D devices are implantable devices equipped to provide CRT along with defibrillation capability.
CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing”. See, also, U.S. Patent Application No. 2008/0306567 of Park et al., entitled “System and Method for Improving CRT Response and Identifying Potential Non-Responders to CRT Therapy” and U.S. Patent Application No. 2007/0179390 of Schecter, entitled “Global Cardiac Performance.”
For the purposes of controlling CRT or for detecting and responding to various arrhythmias, the heart rate of the patient is tracked by examining electrical signals that result in the contraction and expansion of the chambers of the heart. The contraction of atrial muscle tissue is triggered by the electrical depolarization of the atria, which is manifest as a P-wave in a surface electrocardiogram (ECG) and as a rapid deflection (intrinsic deflection) in an intracardiac electrogram (IEGM). The contraction of ventricular muscle tissue is triggered by the depolarization of the ventricles, which is manifest on the surface ECG by an R-wave (also referred to as the “QRS complex”) and as a large rapid deflection (intrinsic deflection) within the IEGM. The electrical activation detected by the pacemaker on either the atrial or ventricular channel is the intrinsic deflection arising from that specific chamber. Repolarization of the ventricles is manifest as a T-wave in the surface ECG and a corresponding deflection in the IEGM. A similar depolarization of the atrial tissue usually does not result in a detectable signal within either the surface ECG or the IEGM because it coincides with, and is obscured by, the R-wave. Note that the terms P-wave, R-wave and T-wave initially referred only to features of a surface ECG. Herein, however, for the sake of brevity and generality, the terms are used to refer to the corresponding signals as sensed internally. Also, where an electrical signal is generated in one chamber but sensed in another, it is referred to herein, where needed, as a “far-field” signal. Hence, an R-wave sensed in the atria is a far-field R-wave (FFRW). The misidentification of an FFRW as a P-wave on the atrial channel is referred to herein as FFRW oversensing.
The sequence of electrical events that represent P-waves, followed by R-waves (or QRS complexes), followed by T-waves can be detected within IEGM signals sensed using pacing leads implanted inside the heart. To help prevent misidentification of electrical events and to more accurately detect the heart rate, the stimulation device employs one or more refractory periods and blanking periods. Within a refractory period, the device does not process electrical signals during a predetermined interval of time—either for all device functions (an absolute refractory period) or for selected device functions (a relative refractory period). As an example of a refractory period, upon delivery of a V-pulse to the ventricles, a post-ventricular atrial refractory period (PVARP) is applied to an atrial sensing channel. A first portion of the PVARP comprises a post-ventricular atrial blanking (PVAB) interval (which can also be referred to as an absolute refractory period). The PVAB is primarily provided to prevent the device from erroneously responding to FFRWs on the atrial channel. The PVARP concludes with a relative refractory period during which the pacemaker ignores all signals detected on the atrial channel as far as the triggering or inhibiting of pacing functions is concerned, but not for other functions, such as detecting rapid atrial rates or recording diagnostic information.
Accurate detection of atrial heart rates is required, for example, for the purposes of enabling an automatic mode switch (AMS) wherein the pacemaker switches from a tracking mode such as a DDD to a nontracking mode such as VDI or DDI. More specifically, the pacemaker compares the atrial rate against an atrial tachycardia detection rate (ATDR) threshold and, if it exceeds the threshold, the pacemaker switches from the tracking mode to the nontracking mode. The ATDR threshold is typically set to, e.g. 180 beats per minute (bpm) although this is a programmable value that the physician can select based on the evaluation of the patient. As such, the ATDR can be employed both as a threshold for detecting atrial tachycardia and as a threshold for mode switching. (In some devices, a separate maximum tracking rate (MTR) is specified, which is at least 20 bpm less than the ATDR.)
Note that DDD, VDI, VVI and DDI are standard device codes that identify the mode of operation of the device. The first letter represents the chamber into which a pacing stimulus is delivered (A=atrium, V=ventricle and D=dual or both). The second letter represents that chamber in which sensing or detection can occur with the same interpretation as for the first position. The third position refers to the way the pulse generator responds to a sensed event (I=inhibited where a sensed signal inhibits the delivery of an output pulse to that chamber, T=triggered where a sensed signal triggers delivery of an output pulse. In the third position, D still means dual but refers to dual modes of response). DDD indicates a device that senses and paces in both the atria and the ventricles and is capable of both triggering and inhibiting functions based upon events sensed in the atria and the ventricles. In DDD, a sensed atrial event (P wave) will inhibit the output to the atrial channel but trigger an output to the ventricular channel after a programmable delay. If an R wave is not sensed within the triggered interval, a ventricular output will be delivered at the end of the interval. This is the technologic equivalent of the physiologic PR interval. VVI indicates that the device is capable of pacing and sensing only in the ventricles. The mode of response to a sensed event is inhibition of the ventricular output and resetting of the basic timing interval. VDI is identical to VVI except that it is also capable of sensing intrinsic atrial activity although it can only pace in the ventricle. DDI is identical to DDD except that the device is only capable of inhibiting pacing based upon sensed events, rather than triggering on sensed events. As such, the DDI mode is a nontracking mode precluding it from triggering ventricular outputs in response to sensed atrial events but capable of pacing in both the atrium and ventricle. Numerous other device modes of operation are possible, each represented by standard abbreviations of this type.
Thus, in a DDD pacing system, AMS recognizes when the patient is in an atrial tachycardia such as atrial fibrillation (AF) and switches from a tracking mode to a nontracking mode to prevent the device from attempting to track the high atrial rates associated with the pathologic atrial tachyarrhythmia (AF). Details regarding AMS may be found in the following patents: U.S. Pat. Nos. 5,441,523 and 5,591,214. See also Levine et al., “Implementation of Automatic Mode Switching in Pacesetter's Trilogy DR+ and Affinity DR Pulse Generators,” Herzschr. Elektrophys. 10 (1999) 5, S46-S57. See, also, the AMS techniques described in U.S. Pat. No. 7,272,438 to Kroll et al., entitled “Mode Switching Heart Stimulation Apparatus and Method” and U.S. Pat. No. 7,187,972 to Fain et al., entitled “Bi-ventricular Pacing in the Face of Rapidly Conducting Atrial Tachyarrhythmia.”
See, also, U.S. Pat. Nos. 7,146,213, 7,158,829, 7,174,210 and 7,184,834 to Levine, each entitled “Method and Apparatus for Improving Specificity of Tachycardia Detection Techniques in Dual-unipolar and Dual-Bipolar Implantable Cardiac Stimulation Systems.” Also, see, U.S. Pat. No. 7,398,123 to Levine, entitled “Methods and devices for reducing the detection of inappropriate physiologic signals to reduce misdiagnosis of normal rhythms as tachyarrhythmias.”
Issues can arise when CRT is delivered by a device equipped for responding to supraventricular tachyarrhythmias with AMS, particularly within devices employing quadra-pole or other multi-pole LV leads, i.e. within devices equipped to deliver multisite CRT. With Multisite LV (MSLV) CRT, pacing stimuli are selectively delivered to the LV at various locations using a set of electrodes distributed along the LV lead or on multiple LV leads in different sites. (This stimulus is synchronized with stimulus pulses delivered to the RV using, e.g., an otherwise conventional bipolar RV lead.) MSLV pacing stimuli and residual charge may be associated with complexes that can be sensed in the atria (i.e. FFRWs sensed on an atrial sensing channel). In at least some devices, due to complications involving hardware discharge and hardware limitations, the net effect during MSLV is one relatively long overall PVAB in the range of, e.g., 130-150 milliseconds (ms) This relatively long PVAB can interfere with the capability of the device to detect and respond to various organized atrial tachycardias (OATs), such as atrial flutter by blinding the system to some of the atrial events. In particular, the relatively long PVAB can prevent the device from properly distinguishing an OAT from a high sinus rate, as might occur during patient exercise, or from sinus rates that only appear to be high due to FFRW oversensing. (A state-of-the-art lead, such as the OptiSense™ lead of St Jude Medical, can help minimize FFRW oversensing, but might not eliminate the phenomenon entirely. In addition, the pulse generator may be connected to an older generation atrial lead, which does not have the same capability to minimize detection of FFRWs).
With regard to atrial flutter, the relatively long PVAB associated with MSLV could preclude detection of every other flutter wave. Circumstances can arise where the device treats this rhythm as a sinus tachycardia resulting in tracking the atrium and a sustained high ventricular paced rate that can aggravate or precipitate overt heart failure due to the sustained high rate pacing, despite any on-going CRT. Conversely, too short a PVAB can predispose the device to FFRW oversensing and inappropriate mode switching.
Accordingly, it would be desirable to provide techniques for controlling MSLV pacing, particularly in conjunction with AMS, which address these and other concerns.